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CMB2004 > L1-4 > Flashcards

L1-4 Flashcards

1
Q

PATHOGENS

A

organisms causing disease

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2
Q

immune system requirements

A

recognition and response
correct reaction to benign/ self
direction of effector mechanisms to specific pathogens
adapative and innate linkage

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3
Q

infection sources

A

pathogens
bacteria
fungi
parasites (worms/ protozoa)

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4
Q

specific immunity features

A

lymphocyte mediation
clonal dist. of receptors
large repertoire/ low freq specific cells for antigen
slow response development of memory cells

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5
Q

clonal selection theory

A

clonal deletion of self-reactive immature lymphocytes
mature naive lymphocytes proliferate and differentiate upon activation
effector cells clones

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6
Q

BCR

A

expressed by B cells upon antibody activation
Ig membrane form binds free antigen

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7
Q

TCR

A

membrane-form only
recognizes peptide fragment of antigen bound to MHC on APC

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8
Q

bacterial infection response

A

complement activation> opsonization/ classical pathway activation/ effector cell activation

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9
Q

FcR cells

A

receptor binding Fc antibody region

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10
Q

antibody structure

A

4 polypeptides
paired variable regions
constant regions > form Fc regions/ receptors
heavy/ light chain

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11
Q

antibody classes

A

IgM/D/A/G/E

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12
Q

What are antibody classes determined by

A

heavy chain/ C region

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13
Q

no. homology regions in L/H regions

A

L>2
H>4/5

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14
Q

homology domain

A

110 amino acids
2 beta sheets
disulphide bridge link
paired (folded in protein)

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15
Q

antibody antigen interaction

A

variable region specific to antibodies
6 hypervariable loops (3Vh/Vl) act as Ag binding sites > 12 regions

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16
Q

CDR on antibody

A

complementarity defining regions
> determines specificity/ affinity for Ag

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17
Q

antigen binding of CDRs

A

Ag bind amino acids in complementarity defining regions

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18
Q

epitope

A

antibody recognition site on an antigen

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19
Q

2 types of epitope

A

linear/ continuous
non-linear

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20
Q

Ag/Ab interactions nature

A

non-covalent

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21
Q

TCR

A

binds processed antigens in cleft of MHC I/II (Peptide-MHC complex)
Membrane-bound
smaller than BCR

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22
Q

TCR structure

A

alpha/ beta chain heterodimer
V/C regions (V peptide bound)
4 Ig-like domains
3 CDR’s

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23
Q

HLA

A

human leukocyte antigens
A/B/C alpha chains
class I/II
on ch6
7*10^6 bp

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24
Q

class I MHC

A

single chain
expressed by all nuc cells
alpha/ beta 2 microglobulin
bind peptides 8-10 amino acids for TCR presentation

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25
Q

class II MHC

A

alpha/ beta chain heterodimer expressed on APC
expressed by immune cells
binds peptides 13+ amino acids

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26
Q

variation in MHC class I/II

A

highly polymorphic
limited variation in one individual

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27
Q

variation of TCR

A

highly variable
clonally distributed

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28
Q

antibody

A

H2L2
secreted/ expressed on B cells
binds free Ag

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29
Q

variability of antibodies

A

highly variable
clonally distributed

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30
Q

alpha 2/ beta 2 coding

A

Ig-like

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31
Q

alpha 1/ beta 1

A

peptide binding site

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32
Q

MHC 1 vs II groove length

A

groove II is more open than I as binds longer peptides

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33
Q

co-expression of TCR recognizing class I

A

CD8+ killer T

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34
Q

co-expression of TCR recognizing class II

A

CD4+ helper T

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35
Q

whats the V region of the heavy chain Ig encoded by

A

V/D/J segments

V (Variable) D (diversity) J(joining)

V is biggest segment

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36
Q

What’s the light chain variable region encoded by?

A

V/J

less variability than heavy chain > V/d/J

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37
Q

Which T cell receptor is the heavy vs light chain?

A

Heavy chain = TCR alpha
light chain = TCR beta

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38
Q

B cell gene rearrangements

A

in bone marrow development

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39
Q

NHEJ

Non-homologous end joining

A

DNA repair ligating DNA pairs

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40
Q

light chain genes

A

lamda/ kappa

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41
Q

Loci of H/ lamda/ kappa genes

A

H- 14
lamda- 2
kappa- 22

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42
Q

recombination signal sequences

A

sequences flanking V/D/J gene segments

V/D/J recombinases

recombination activating genes 1/2 encoding lymphoid specific components of recombinase

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43
Q

RAG mutations consequences

recombination activating gene

A

immunodeficiences

44
Q

Allelic exclusion

A

per B> 1 rearranged H and 1 rearranged L chain per chromosomes therefore randomly generated BCR

kappa OR lamda light chain never both

45
Q

mechanisms for allelic exclusion

A
  1. multiple gene segments/ chain
  2. combinatorial diversity
  3. H/L chain combinations
  4. junctional diversity
  5. somatic hypermutations

2. V/D/J segment recomination

46
Q

junctional diversity

A

imprecise joining
N regions

random nuc additions at junctions via terminal transferase

47
Q

SHM

somatic hypermutation

A

mutation frequency in antibody H/ lamda/ kappa genes at orders of magnitude higher than others

in germinal centers as B recognize Ag asnd proliferate

48
Q

AID

Activation induced deaminase

A

deaminates DNA cytosine to uracil which is recognized

49
Q

Mechanism induced by B recognition of Ag

A

secrete unique BCR as Ig with alternate constant region w/o transmembrane region

both produced by alternative RNA processing

50
Q

heavy chain constant region genes

A

4* gamma chain gene
2*alpha chain gene segments

C mu closest to V/D/J gene segments

51
Q

IgM

A

1st class isotype BCR/ antibody expressed by each developing B cell

co-expressed with IgD

52
Q

TCR gene segment rearrangement

when/ where

how is it similar to Ig gene rearrangement?

A

During T development in thymus

similar to Ig gene rearrangement> RSS/ RAG enzymes involved

53
Q

diversity of TCR rearrangement

A
  1. multiple gene segments
  2. combinatorial diversity
  3. junctional diversity

no SHM in TCRs

54
Q

TCR alpha/beta chromosomes

A

alpha-14
beta- 7

55
Q

where do TCR’s recognize antigens

A

in groove of MHC moelcule

56
Q

MHC diversity

major histocompatibility complex

which chromosome is HLA gene found on?

A

no gene rearrangement
co-dominant expression

most polymorphic genes

Ch 6

57
Q

Co-dominant expression of MHC

Where are these expressed?

A

MHC I
MHC II

1 in all nucleated cells
II in immune cells

58
Q

MHC I molecules
MHC class II molecules

No. molecules if heterozygous at each loci?

A

MHCI> HLA-A/HLA-B/HLA-C
MHCII> HLA-DQ/DP/DR

6

59
Q

MHC polymorphism

advantages/ disadvantages

A

:) allows binding of peptide range presented to cells
:( ^risk of immune-mediated disease
:( lower donor organ pool

60
Q

endogenous/ exogenous Ag-derived peptides

A

endo> virus (class I presented)
exo> bacterium/ fungus (class II presented)

both processed into fragments for binding/ presentation by MHC I/II

61
Q

MHC class I presentation

A
  1. intra antigen synth in ctoplasm
  2. Ag processed > peptide by proteasome
  3. TAP transporter to ER
  4. pep binding to MHC I
  5. MHC I presentation at CSM
62
Q

proteasome

A

inflam cytokine reception produces altered peptides
large multicatalytic protease

63
Q

what’s TAP

A

Multi-protein assembly / peptide loading component

contains tapasin/ calreticulin

64
Q

TAP functions

A

cytosolic protein degradation to peptide fragments by proteasome
delivers peptide to MHC Class I and folds for export

65
Q

MHC class II molecule presentation

A
  1. Ag endocytosed via vesicles
  2. acid proteases cleave protein
  3. vesicles fuse with MHC II and bind
  4. complex transported to CSM
66
Q

invariant chain complex in MHC II

function

A

blocks peptide/ misfolded protein binding in groove

HLA-DM binds

cleaved in acidified endosome > peptide fragment CLIP enzyme

67
Q

CLIP function

A

blocks peptide binding ass. w binding groove

released when HLA-DM binds to MHC II

68
Q

what happens to peptides in normal, uninfected cells?

A

MHC I/ II bind and present peptides from self-proteins

69
Q

class I/II MHC accessory molecules encoded

A

class I> TAP/LMP
class II> HLA-DM

70
Q

where are B cells and plasma cells found?

A

in bone marrow

71
Q

gene controlling B cell identity

A

Pax5

72
Q

B cell development

A
  1. develop from haematopoietic stem cells in bone marrow
  2. express PAX5 txn factor
  3. Ig gene rearrangement
  4. lymphocyte then B cell- specific markers expressed
  5. negative selection of self-reactive cells
73
Q

Pre-B cell development

immature pre-B cells

A
  1. H chain genes rearrange to cell surface with Igalpha/beta> expressed with surrogate light chain
    produces a pre B cell receptor
  2. L chains rearrange > displace V pre-B / lamda 5 genes and producing IgM BCR

H chain = mu chain

74
Q

Pre-B cell receptor function

A

delivers signal to pre-B cells that H chain is functional nctional

no antigen required

75
Q

Pre-BCR signal

A
  1. turns off RAG1/RAG2
  2. 5-6 cell divisions
  3. surrogate light chain expression stops
  4. RAG1/2 turned on again
  5. L chain rearrangement

L chain rearrangement requires RAG

76
Q

Ig alpha/ beta function

A

mediate signalling of immature B cells

77
Q

B cell names during development

A

stem cell> early pro B cell> pro B cell> large pre-B cell> small pre B cell> immature B cell> mature B cell

78
Q

light chain posiibilities from pre-B cells

A

lamda or kappa light chain

79
Q

kappa versus lamda expression on light chains

A

more kappa than lamda as kappa light chains rearraneg prior to lamda

80
Q

where are RAG1/2 switched off?

A

large pre-B cell/ mature B cells

lymphoid specific recombinase

81
Q

no. J(kappa) genes per chromosome

A

5 per chromosome

and 2 chromosomes therefore 10 rearrangements possible on same locus

lamda locus will then rearrange if all 10 rearrangements are out of frame

82
Q

Ig rearrangement errors consequences

A

failure to productively rearrange H and L chains result in cell death

83
Q

Ig rearrangement sequence

A

D-J on both chromosomes
V-DJ on 1/2 chromosomes
kappa gene rearrangement (up to 5 times) on 1/2 chromosomes> rearrangement of lamda if kappa fails on 1/2 chromosomes
mu: kappa/lamda expressed

84
Q

Ig expressed in immature B cells

A

membrane IgM

85
Q

what happens to immature B cells binding multivalent self-antigens?

A

clonal deletion
receptor editing

receptor ediitng entails further light chain rearrangements/ variable ge

86
Q

what happens to immature B cells binding soluble self-antigens?

A

become anergic/ unresponsive

87
Q

T cell development

A

Develop from bone marrow stem cells
receptor genes rearranged in thymus
pre-T receptor expressed
negative selection of self-reactive T cells

88
Q

T cell alternative lineages

A

alpha beta TCR genes (CD4+/CD8+)
gamma delta TCR genes

cells expressing alpha beta TCR bind with self MHC expressed in thymus (

89
Q

alpha beta T cell development

A

develop into thymocytes in thymus
1. beta TCR genes rearranged and express TCR
2. CD3/4/5 markers acquired\
3. +/- selection

90
Q

thymus characteristics

A

bi-lobed organ in anterior mediastinum
outer cortex/ innor medulla per lobule
made up of dendritic/ macrophage/ epithelial / lymphoid cells

pro-thymocytes enter cortex via blood vessels from bone marrow

91
Q

thymocyte TCR rearrangement

A
  1. TCR beta rearranged
  2. expression w pre-beta receptor
  3. cell proliferationa nd TCR beta rearrangement
92
Q

markers expressed w TCR

A

CD3
CD4 and CD8

peripheral T Cells express either CD4 or CD8

93
Q

CD3 function

A

transmits signal to T cell nucleus after TCR recognition of p/ MHC

93
Q

TCR expression requirements

A

CD3 complex
delta, epsilon and gamma chains
zeta chain dimer

94
Q

gamma delta TCR

A

less diverse TCR
don’t express CD4/CD8
in epithelial tissues at mucosal surfaces

lineage commitment to gamma delta/ alpha beta depends on order of intial rearrangements

95
Q

immunity T cell recognition

A

recognize self-MHC + foreign Ag peptide

positively selected and moved to medulla

96
Q

autoimmunity T cell recognition

A

Recognize self-MHC + peptide from self

positively selected and moved to medulla prior to removal by negative se

clonal deletion with those with highest affinity for TCR neg. selected

97
Q

positive selection of T cells

A

T cells recognize MHC on cortical epithelial cells in thymus
positively selected move to medulla

apoptosis if no recognition

97
Q

negative selection of T cells

A

on thymic dendritic cells/ macrophages w high affinityTCR negatively selected

therefore population of T cells w low affinity for self-peptide + self-MHC

98
Q

CD 8 + T cells

A

recognize MHC class I Ag

99
Q

CD4+ T cells

A

recognize MHC class II Ag

100
Q

what type of proteins are BCRs?

A

heterodimeric

101
Q

Do TCRs recognise carbohydrate?

A

no

102
Q

MHC I/II binding groove

A

I snaps shut on smaller peptides in ER following TAP translocation
II has binding groove blocked by CLIP (removed in endocytic pathway by HLA-DM)

103
Q

which chain determines an antibody’s isotype?

A

heavy

104
Q
A

CMB2004 (4 decks)

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